2,5-Anhydro-D-mannitol
(Synonyms: 2,5-脱水-D-甘露醇) 目录号 : GC41470
An antimetabolic fructose analogue
Cas No.:41107-82-8
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >95.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
2,5-Anhydro-D-mannitol is an antimetabolic fructose analogue that increases food intake in rats at doses of 50-800 mg/kg by inhibiting gluconeogenesis and glycogenolysis in the liver.. It is phosphorylated in the liver, which decreases available ATP and signals eating behavior in rats through a vagal nerve mechanism.
| Cas No. | 41107-82-8 | SDF | |
| 别名 | 2,5-脱水-D-甘露醇 | ||
| Canonical SMILES | OC[C@@H]1[C@@H](O)[C@H](O)[C@@H](CO)O1 | ||
| 分子式 | C6H12O5 | 分子量 | 164.2 |
| 溶解度 | DMF: 25 mg/ml,DMSO: 30 mg/ml,Ethanol: 5 mg/ml,PBS (pH 7.2): 10 mg/ml | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 6.0901 mL | 30.4507 mL | 60.9013 mL |
| 5 mM | 1.218 mL | 6.0901 mL | 12.1803 mL |
| 10 mM | 0.609 mL | 3.0451 mL | 6.0901 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Inhibition of gluconeogenesis and glycogenolysis by 2,5-Anhydro-D-mannitol
J Biol Chem 1984 Jan 10;259(1):218-23.PMID:6423625doi
2,5-Anhydro-D-mannitol (100 to 200 mg/kg) decreased blood glucose by 17 to 58% in fasting mice, rats, streptozotocin-diabetic mice, and genetically diabetic db/db mice. Serum lactate in rats was elevated 56% by 2,5-Anhydro-D-mannitol, but this could be prevented by dichloroacetate (200 mg/kg) or thiamin (200 mg/kg). In hepatocytes from fasted rats, 1 mM 2,5-Anhydro-D-mannitol inhibited gluconeogenesis from a mixture of alanine, lactate, and pyruvate. It also inhibited glucose production and stimulated lactate formation from glycerol or dihydroxyacetone. Glycogenolysis in hepatocytes from fed rats was markedly inhibited by 1 mM 2,5-Anhydro-D-mannitol both in the presence or absence of 1 microM glucagon. 2,5-Anhydro-D-mannitol can be phosphorylated by fructokinase or hexokinase to the 1-phosphate and then by phosphofructokinase to the 1,6-bisphosphate. Rat liver glycogen phosphorylase was inhibited by 2,5-Anhydro-D-mannitol 1-phosphate (apparent Ki = 0.66 +/- 0.09 mM) but was little affected by 2,5-Anhydro-D-mannitol 1,6-bisphosphate. Rat liver phosphoglucomutase was inhibited by 2,5-Anhydro-D-mannitol 1-phosphate (apparent Ki = 2.8 +/- 0.2 mM), whereas 2,5-Anhydro-D-mannitol 1,6-bisphosphate served as an alternative activator (apparent K alpha = 7.0 +/- 0.5 microM). Rabbit liver pyruvate kinase was activated by 2,5-Anhydro-D-mannitol 1,6-bisphosphate (apparent K alpha = 9.5 +/- 0.9 microM), whereas rabbit liver fructose 1,6-bisphosphatase was inhibited by 2,5-Anhydro-D-mannitol 1,6-bisphosphate (apparent Ki = 3.6 +/- 0.3 microM). The phosphate esters of 2,5-Anhydro-D-mannitol would, therefore, be expected to inhibit glycogenolysis and gluconeogenesis and stimulate glycolysis in liver.
Effects of GLP-1 and 2,5-Anhydro-D-mannitol on insulin secretion and plasma glucose in mice
Endocr Res 1995 Aug;21(3):583-94.PMID:7588428DOI:10.1080/07435809509030475.
The truncated glucagon-like peptide-1 (GLP-1(7-36)amide or GLP-1) stimulates insulin secretion, enhances glucose elimination and is of potential interest in diabetes treatment. We studied the hypoglycemic action of GLP-1 in normal mice when given alone or together with the fructose analogue, 2,5-Anhydro-D-mannitol (2,5-AM), which inhibits glycogenolysis and gluconeogenesis. GLP-1 (32 nmol/kg iv) lowered plasma glucose levels after 25 min to 4.6 +/- 0.2 mmol/l compared with 7.3 +/- 0.4 mmol/l in controls (P < 0.001). Also 2,5-AM (0.5 mumol/kg iv) reduced plasma glucose levels, to 5.6 +/- 0.3 mmol/l (P < 0.01). When given together, the glucose lowering action of GLP-1 and 2,5-AM was additive, since the 25 min glucose level was 2.8 +/- 0.2 mmol/l. At 5 min after injection, GLP-1 had increased plasma insulin levels to 693 +/- 68 pmol/l compared with 342 +/- 42 pmol/l in controls (P < 0.01). 2,5-AM abolished this increase. Furthermore, GLP-1 (32 nmol/kg) did not affect the glycogen content, neither in the liver nor in the gastrocnemic muscle in samples taken at 30 min after injection. Moreover, in isolated islets incubated at 3.3 and 8.3 mmol/l glucose, 2,5-AM at 75 mmol/l inhibited glucose-stimulated insulin secretion (P < 0.05) showing that 2,5-AM inhibits insulin secretion both in vivo and in vitro. We conclude that GLP-1 may reduce plasma glucose levels also to levels below the basal levels under normal conditions, and that an insulin- and liver-independent action of the peptide contributes to its hypoglycemic action in normal animals.
2,5-Anhydro-D-mannitol: a fructose analogue that increases food intake in rats
Am J Physiol 1988 Jan;254(1 Pt 2):R150-3.PMID:3122594DOI:10.1152/ajpregu.1988.254.1.R150.
We examined the effects on food intake and plasma fuels of 2,5-Anhydro-D-mannitol (2,5-AM; 2-deoxy-D-fructose), a fructose analogue that inhibits hepatocyte gluconeogenesis and glycogenolysis in vitro. 2,5-AM (50-800 mg/kg po) given to rats during the diurnal fast produced a dose-related increase in food intake during the 2 h after administration. A 200-mg/kg dose of 2,5-AM decreased plasma glucose, increased plasma ketone bodies, free fatty acids, and glycerol, and had no effect on triglycerides. Normal and diabetic rats given 2,5-AM (200 mg/kg ip) increased food intake to the same extent. These results suggest that, unlike other substrate analogues that increase food intake, 2,5-AM increases feeding by creating a metabolic state that resembles fasting.
2,5-Anhydro-D-mannitol: its unique central action on food intake and blood glucose in rats
Brain Res 1991 Dec 6;566(1-2):270-5.PMID:1814543DOI:10.1016/0006-8993(91)91708-9.
Peripheral administration of D-fructose has been reported to decrease food intake, and its 2-deoxy analogue, 2,5-Anhydro-D-mannitol (2,5-AM), increased food intake and decreased blood glucose in rats. In the present study, 2,5-AM was selected for comparison with well-known 2-deoxy analogues of glucose. Infusion of 2,5-AM into the rat third cerebroventricle at 11.00 h induced feeding dose dependently (Y = 0.63 logX-1.20, r = 0.95, P less than 0.05). Rats treated with 2,5-AM at a maximal effective dose of 24 mumol/rat ate meals most persistently (P less than 0.05). No periprandial drinking was observed. Ambulatory activity increased concomitantly with feeding, but did not exceed the activity normally associated with a meal. Infusion of 24 mumol 2,5-AM into the third cerebroventricle induced no substantial change in plasma glucose or insulin in any 60-min experimental period. Unilateral microinfusion of 1.2 mumol 2,5-AM induced feeding in all 6 rats (P less than 0.01) when a cannula tip was located in the ventromedial hypothalamic nucleus (VMH), but not in the lateral hypothalamic area (LHA). These findings indicate that feeding elicitation may be due to disinhibition by 2,5-AM through the VMH. This is quite unique compared to the action mechanisms of hexose, pentose and their analogues, except 2,5-AM.
2,5-Anhydro-D-mannitol induces Fos-like immunoreactivity in hindbrain and forebrain: relationship to eating behavior
Brain Res 1998 Jan 1;779(1-2):17-25.PMID:9473567DOI:10.1016/s0006-8993(97)01073-1.
Injection of the fructose analogue, 2,5-Anhydro-D-mannitol (2,5-AM), stimulates eating behavior in rats. Previous studies have shown that administration of 2,5-AM in doses that elicit eating induces Fos-like immunoreactivity (Fos-li) primarily in hindbrain structures, including the nucleus of the solitary tract (NTS), area postrema (AP), and lateral parabrachial nucleus (PBN). To more closely assess the relationship between neural activation and the eating response to 2,5-AM treatment, we measured food intake and brain Fos-li in rats given a range of doses of 2,5-AM. The numbers of neurons showing Fos-li were quantified by computerized image analysis. Doses of 2,5-AM that reliably stimulated food intake induced Fos-li in both the hindbrain and forebrain, including in the NTS, AP, lateral PBN, central lateral nucleus of the amygdala, dorsal lateral bed nucleus of the stria terminalis (BNSTdl), anterior paraventricular nucleus of the thalamus, supraoptic nucleus, subfornical organ, and paraventricular hypothalamic nuclei. A low dose of 2,5-AM that did not elicit eating increased Fos-li marginally only in the AP, PBN, and BNSTdl. The results suggest that 2,5-AM treatment activates a vagal afferent pathway projecting from the hindbrain to forebrain that is involved in initiating the eating response to the fructose analogue.